Identifying heart failure patients suitable for resynchronization therapy using qrs complex width from an intracardiac electrogram

ABSTRACT

Methods and systems are disclosed for determining whether a patient is a responder to cardiac resynchronization therapy. The beginning and ending of the intrinsic ventricular depolarization are determined through signals measured from one or more electrodes implanted in the patient&#39;s heart. An interval between the beginning and ending of the intrinsic ventricular depolarization is computed and is compared to a threshold. The threshold may be determined empirically. The pacing parameters of a heart stimulation device, such as a pacemaker, may then be configured, for example, by setting the paced atrio-ventricular delay based on whether the patient responds positively to cardiac resynchronization therapy.

CLAIMS OF PRIORITY

This application is a continuation of U.S. application Ser. No.12/221,650, filed on Aug. 5, 2008, which is a continuation of U.S.application Ser. No. 11/133,526, filed on May 20, 2005, now issued asU.S. Pat. No. 7,424,324,which is a continuation of U.S. application Ser.No. 10/008,397, filed on Dec. 6, 2001, now issued as U.S. Pat. No.6,993,389, which is a continuation-in-part of U.S. application Ser. No.09/822,790 filed on Mar. 30, 2001, now issued as U.S. Pat. No. 6,766,189and is also a continuation-in-part of the U.S. application Ser. No.09/822,638 also filed on Mar. 30, 2001, now issued as U.S. Pat. No.6,705,999.

TECHNICAL FIELD

The present invention is directed to cardiac resynchronization therapy.More specifically, the present invention is directed to methods andsystems for detecting whether patients are responders to ventricularresynchronization therapy.

BACKGROUND

The heart is a muscular organ comprising multiple chambers that operatein concert to circulate blood throughout the body's circulatory system.As shown in FIG. 1, the heart 100 includes a right-side portion or pump102 and a left-side portion or pump 104. The right-side portion 102includes a right atrium 106 and a right ventricle 108. Similarly, theleft-side portion 104 includes a left atrium 110 and a left ventricle112. Oxygen-depleted blood returning to the heart 100 from the bodycollects in the right atrium 106. When the right atrium 106 fills, theoxygen-depleted blood passes into the right ventricle 108 where it canbe pumped to the lungs (not shown) via the pulmonary arteries 117.Within the lungs, waste products (e.g., carbon dioxide) are removed fromthe blood and expelled from the body and oxygen is transferred to theblood. Oxygen-rich blood returning to the heart 100 from the lungs viathe pulmonary veins (not shown) collects in the left atrium 110. Thecircuit between the right-side portion 102, the lungs, and the leftatrium 110 is generally referred to as the pulmonary circulation. Whenthe left atrium 110 fills, the oxygen-rich blood passes into the leftventricle 112 where it can be pumped throughout the entire body. In sodoing, the heart 100 is able to supply oxygen to the body and facilitatethe removal of waste products from the body.

To circulate blood throughout the body's circulatory system as describedabove, a beating heart performs a cardiac cycle that includes a systolicphase and a diastolic phase. During the systolic phase (e.g., systole),the ventricular muscle cells of the right and left ventricles 108, 112contract to pump blood through the pulmonary circulation and throughoutthe body, respectively. Conversely, during the diastolic phase (e.g.,diastole), the ventricular muscle cells of the right and left ventricles108, 112 relax, during which the right and left atriums 106, 110contract to force blood into the right and left ventricles 108, 112,respectively. Typically, the cardiac cycle occurs at a frequency between60 and 100 cycles per minute and can vary depending on physical exertionand/or emotional stimuli, such as, pain or anger.

The contractions of the muscular walls of each chamber of the heart 100are controlled by a complex conduction system that propagates electricalsignals to the heart muscle tissue to effectuate the atrial andventricular contractions necessary to circulate the blood. As shown inFIG. 2, the complex conduction system includes an atrial node 120 (e.g.,the sinoatrial node) and a ventricular node 122 (e.g., theatrioventricular node). The sinoatrial node 120 initiates an electricalimpulse that spreads through the muscle tissues of the right and leftatriums 106, 110 and the atrioventricular node 122. As a result, theright and left atriums 106, 110 contract to pump blood into the rightand left ventricles 108, 112 as discussed above. At the atrioventricularnode 122, the electrical signal is momentarily delayed beforepropagating through the right and left ventricles 108, 112. Within theright and left ventricles 108, 112, the conduction system includes rightand left bundle branches 126, 128 that extend from the atrioventricularnode 122 via the Bundle of His 124. The electrical impulse spreadsthrough the muscle tissues of the right and left ventricles 108, 112 viathe right and left bundle branches 126, 128, respectively. As a result,the right and left ventricles 108, 112 contract to pump blood throughoutthe body as discussed above.

Normally, the muscular walls of each chamber of the heart 100 contractsynchronously in a precise sequence to efficiently circulate the bloodas described above. In particular, both the right and left atriums 106,110 contract (e.g., atrial contractions) and relax synchronously.Shortly after the atrial contractions, both the right and leftventricles 108, 112 contract (e.g., ventricular contractions) and relaxsynchronously. Several disorders or arrhythmias of the heart can preventthe heart from operating normally, such as, blockage of the conductionsystem, heart disease (e.g., coronary artery disease), abnormal heartvalve function, or heart failure.

Blockage in the conduction system can cause a slight or severe delay inthe electrical impulses propagating through the atrioventricular node122, causing inadequate ventricular relaxations and filling. Insituations where the blockage is in the ventricles (e.g., the right andleft bundle branches 126, 128), the right and/or left ventricles 108,112 can only be excited through slow muscle tissue conduction. As aresult, the muscular walls of the affected ventricle (108 and/or 112) donot contract synchronously (e.g., asynchronous contraction), thereby,reducing the overall effectiveness of the heart 100 to pump oxygen-richblood throughout the body. For example, asynchronous contraction of theleft ventricular muscles can degrade the global contractility (e.g., thepumping power) of the left ventricle 112 which can be measured by thepeak ventricular pressure change during systole (denoted as “LV+dp/dt”).A decrease in LV+dp/dt corresponds to a worsened pumping efficiency andless cardiac output.

Similarly, heart valve disorders (e.g., valve regurgitation or valvestenosis) can interfere with the heart's 100 ability to pump blood,thereby, reducing stroke volume (i.e., aortic pulse pressure) and/orcardiac output.

Various medical procedures have been developed to address these andother heart disorders. In particular, cardiac resynchronization therapy(“CRT”) can be used to improve the conduction pattern and sequence ofmechanical contractions of the heart. CRT involves the use of anartificial electrical stimulator that is surgically implanted within thepatient's body. Leads from the stimulator can be affixed at a desiredlocation within the heart to effectuate synchronous atrial and/orventricular contractions. Typically, the location of the leads (e.g.,stimulation site) is selected based upon the severity and/or location ofthe blockage. Electrical stimulation signals can be delivered toresynchronize the heart, thereby, improving cardiac performance.

Despite these advantages, several shortcomings exist that limit theusefulness of CRT. For example, results from many clinical studies haveshown that hemodynamic response to CRT typically varies from patient topatient, ranging from very positive (e.g., improvement) to substantiallynegative (e.g., deterioration). Thus, in order to predict the benefitfrom CRT, the patient typically must be screened prior to receiving thetherapy. One common method that predicts hemodynamic response to CRTrelies on measurement of a surface electrocardiagram (ECG). Suchmeasurement is often performed manually and is subject to human error.Additionally, it is difficult to implement such a surface measurementwith an implantable device thereby making it difficult to continuouslymonitor the response.

Thus, there is a need for improved methods and systems that canautomatically and reliably predict whether a patient will have apositive response to CRT and/or be able to monitor the responsecontinuously during the entire course of CRT.

SUMMARY

Embodiments of the present invention provide methods and systems thatdetect whether a patient is a responder to CRT. The methods and systemsinvolve making measurements with at least one electrode implanted withinthe patient's heart. An implanted heart stimulation device, externaldevice programmer, or other device may then determine from themeasurements whether the patient will have a positive response to CRT.

The present invention may be viewed as a method for determining whethera patient is a responder to resynchronization therapy. The methodinvolves detecting a beginning of an intrinsic ventriculardepolarization with an electrode positioned at a ventricle of the heartof the patient. An ending of the intrinsic ventricular depolarization isalso detected. An interval between the beginning of the intrinsicventricular depolarization and the ending of the intrinsic ventriculardepolarization is measured. The interval is then compared to athreshold.

The present invention may also be viewed as a system for determiningwhether a patient is a responder to resynchronization therapy. Thesystem includes an electrode positioned at a ventricle of the heart ofthe patient. A detection module is communicatively linked to theelectrode, and the detection module detects a beginning of an intrinsicventricular depolarization and an ending of the intrinsic ventriculardepolarization. The system also includes a processing modulecommunicatively linked to the detection module, wherein the processingmodule computes an interval between the beginning of the intrinsicventricular depolarization and the ending of the intrinsic ventriculardepolarization and compares the interval to a threshold.

The present invention may also be viewed as another system fordetermining whether a patient is a responder to resynchronizationtherapy. The system includes means for detecting a beginning of anintrinsic ventricular depolarization and an ending of the intrinsicventricular depolarization. Additionally, the system includes means forcomputing an interval between the beginning of the intrinsic ventriculardepolarization and the ending of the intrinsic ventriculardepolarization and for comparing the interval to a threshold.

DESCRIPTION OF THE DRAWINGS

FIG. 1 is a diagram showing the various chambers of the heart.

FIG. 2 is a diagram showing the various chambers and the electricalconduction system of the heart.

FIG. 3 is a graph showing ventricular depolarization as a function oftime.

FIGS. 4-6 are diagrams illustrating a heart and the electricalconduction system advancing through a normal cardiac cycle.

FIG. 7 is a graph illustrating mean percentage change in leftventricular pressure (LV+dp/dt) resulting from application of CRTplotted against the duration of intrinsic ventricular depolarization forresponders and non-responders.

FIG. 8 is a graph illustrating the accuracy, sensitivity, andspecificity of the separation between responders and non-responders forvarious thresholds of ventricular depolarization duration used to makethe distinction.

FIG. 9 illustrates one possible embodiment of a system that can be usedto detect whether a patient is a responder to CRT.

FIG. 10 is an operational flow summarizing the logical operationsemployed by an exemplary system for detecting whether a patient is aresponder to CRT.

DETAILED DESCRIPTION

Various embodiments of the present invention will be described in detailwith reference to the drawings, wherein like reference numeralsrepresent like parts and assemblies throughout the several views.Reference to various embodiments does not limit the scope of the presentinvention, which is limited only by the scope of the claims attachedhereto.

The following discussion is intended to provide a brief, generaldescription of a suitable method for predicting whether a patient willpositively respond to cardiac resynchronization therapy (“CRT”). As willbe described in greater detail below, the method of the presentdisclosure predicts a patient's response to CRT by measuring andcomparing an intrinsic ventricular depolarization period against athreshold. As will become apparent from the discussion below inconnection with the various drawings, the ventricular depolarizationperiod may be measured by finding a beginning and ending of thedepolarization through processing of an intracardiac signal to find abeginning value Q* and an ending value S*. However, those of ordinaryskill in the art will readily appreciate that the method of the presentdisclosure can be implemented using any suitable beginning and endingvalue, which may or may not be found by employing various methods formeasuring Q* and S*.

In a preferred embodiment, the method of the present disclosure predictswhether a patient will respond to CRT by evaluating the period ofdepolarization of the right or left ventricles 108, 112 (FIG. 1). Theperiod of depolarization of the ventricles 108, 112 can be evaluatedusing an intracardiac electrogram. An intracardiac electrogram isgenerally a graphical depiction of the electrical depolarization orexcitement of the heart 100 (FIG. 1) that is measured by one or moreelectrodes placed on or within the heart 100, such as within the rightor left ventricles.

An exemplary electrogram for an intrinsic systolic cycle is shown inFIG. 3. Each portion of the electrogram is typically given an alphabeticdesignation corresponding to a pre-determined period of electricaldepolarization or excitement. For example, the portion of theelectrogram that represents atrial depolarization is commonly referredto as the P-wave (not shown). Similarly, the portion of the electrogramthat represents ventricular depolarization is commonly referred to asthe QRS complex comprising a Q-wave, an R-wave, and an S-wave. Moreover,the portion of the electrogram that represents ventricular recovery orrepolarization is commonly referred to as the T-wave (not shown).

As shown in FIG. 3, the QRS complex has a beginning and an ending. Todetermine the beginning and ending, the intracardiac electrogram may beanalyzed, as discussed below, to find various representative values. Therepresentative beginning value Q* and ending value S* are shown in FIG.3. Other values representative of the beginning and ending of the QRScomplex may be used in place of the Q* and S* values that are defined bythe calculations discussed below.

Each period of electrical depolarization or excitement represented onthe electrogram corresponds to a period of muscular activation withinthe heart 100 (FIG. 1). FIGS. 4-6 are schematic illustrations depictingthe various periods of muscular activation within the heart 100. Asshown in FIGS. 4-6, the electrogram data can be monitored using anysuitable electrocardiographic device 150, such as an implantable heartstimulation device (i.e. CRT device), that is connected to leads locatedon or within the heart 100.

FIG. 4 is a schematic illustration showing the period of atrialactivation in response to electrical impulses initiated at thesinoatrial node 120 (corresponding to the P-wave portion as discussedabove). After electrical impulses spread from the sinoatrial node 120,the muscle tissues of the right and lee atriums 106, 110 contract topump blood into the right and left ventricles 108, 112, respectively.

FIG. 5 is a schematic illustration showing the period of a ventriculardepolarization in response to electrical impulses initiated at theatrioventricular node 122 that spread through the ventricles 108, 112(corresponding to the QRS portion as discussed above). After electricalimpulses spread from the atrioventricular node 122, the muscle tissuesof the right and left ventricles 108, 112 contract to pump blood to thelungs and throughout the body, respectively.

FIG. 6 is a schematic illustration showing ventricular recovery orrepolarization (corresponding to the T-wave portion as discussed above).During ventricular repolarization, the membrane potential of the musclecells reverse polarity and return to their resting state, thereby,causing the ventricles to relax.

An electrogram of a patient's heart can be used to assess cardiacperformance by validating the existence of cardiac abnormalities, suchas, arrhythmias evinced by an abnormally fast heart rate (e.g.,tachycardia), an abnormally slow heart rate (e.g., bradycardia), or anormal rate but the depolarization is abnormally propagated (e.g.,ectopic, or conduction system defect). The existence of an arrhythmiatypically indicates that the heart's rhythm initiation and/or conductionsystem is functioning abnormally. CRT can be used, among otherapplications, to treat abnormal electrical conduction. In particular,CRT can be used to deliver electrical stimulation to portions of theheart 100 (FIG. 1) to resynchronize the heart's activation, thereby,improving the efficiency of atrial and ventricular contractionsnecessary to circulate blood throughout the body. The amount of benefitderived from CRT, however, typically varies depending upon the severityof the abnormality of the heart's conduction system. Therefore, prior totreating a patient using CRT, it is preferable to evaluate whether theheart's 100 (FIG. 1) conduction system is normal or abnormal.

The heart's ventricular conduction system can be assessed throughanalysis of the duration of ventricular depolarization. Identificationof patients who may have a positive response to CRT can be performedusing the duration of ventricular depolarization (e.g., the width of theQRS complex as shown in FIG. 3) measured from an intracardiacelectrogram. For example, if the duration of ventricular depolarizationis greater than a given threshold, then the patient may be considered aresponder to CRT, and the CRT device for that patient may be configuredappropriately. Patients are referred to as responders because they havean abnormal conduction system that can benefit from CRT.

Once the patient has been deemed a responder or non-responder, the CRTdevice can be configured to stimulate the heart to produce anatrioventricular delay of a duration appropriate for the patient type asis discussed below. For responders, the atrioventricular delay isgenerally set to about one-half of the intrinsic, or naturally occurringatrioventricular delay. For non-responders, the atrioventricular delayis set to approximately the intrinsic atrioventricular delay, such asthe intrinsic atrioventricular delay minus a relatively small delayfactor of about 30 milliseconds. One with ordinary skill in the art willrecognize that other atrioventricular delay settings for responders andnon-responders are possible as well. The atrioventricular delay isgenerally considered to be the length of time between an atrial sensed(or stimulated) event and the delivery of a ventricular output pulse.

FIG. 7 shows a graph of the mean percent change in peak left ventriclepressure “LV+dp/dt” after application of CRT over three atrioventriculardelays for a group consisting of both responders and non-responders.Responders may be defined as those who receive an increase in peak leftventricle pressure when CRT is applied. From the graph, one can see thata relationship exists between the intrinsic Q*S* depolarization intervaland the increase in peak left ventricle pressure due to CRT. For thosehaving a relatively long intrinsic ventricular depolarization, CRTcaused a relatively large increase in peak left ventricle pressure. Forthose having a relatively short intrinsic ventricular depolarization,CRT caused a relatively small increase or in some instances a decreasein peak left ventricle pressure.

A linear regression of the test cases shows that the correlation ofpercent change in peak left ventricle pressure to Q*S* is defined by theequation y=0.3462x−51807, with a coefficient of determination R²=0.3974.The vertical line of FIG. 7 indicates that an appropriate Q*S* thresholdfor distinguishing responders from non-responders is approximately 175milliseconds for humans. The determination of 175 milliseconds as anappropriate threshold is further supported by the plot in FIG. 8.

FIG. 8 shows the values for the accuracy which represents theprobability of correct classification of either a responder ornon-responder, sensitivity which represents the probability of correctclassification of patients as responders, and specificity which is theprobability of correct classification of patients as non-respondersplotted against Q*S* thresholds for humans. From this plot, it can beseen that the optimal threshold is about 175 milliseconds for humansbecause at this point the accuracy and sensitivity are above 0.95 andthe specificity is above 0.88.

One possible embodiment of a CRT system 300 that can be used toimplement the methods for determining whether a patient is a responderis illustrated in FIG. 9. As shown in FIG. 9, the CRT system 300generally comprises a programming device 301 that can be used toregulate stimulation pulses that are delivered to the heart 100. In onepossible embodiment, the heart 100 is connected to various leads 320having electrodes (not shown) and terminal pins (not shown) that canconnect the heart 100 to the CRT system 300. The various leads 320connecting the heart 100 to the CRT system 300 will be described ingreater detail below.

The programmer 301 can regulate the stimulation pulses delivered to theheart 100 using, for example, a telemetry module 302. In one possibleembodiment, the telemetry module 302 is unidirectional (e.g., capable ofallowing the programmer 301 to receive data). However, in an alternativeembodiment, the telemetry module 302 is bi-directional (e.g., capable ofallowing the programmer 301 to receive and/or send data). The commandinput module 304 is configured to interpret the data received from theprogrammer 301 such that the stimulation pulses can be accuratelydistributed according to predetermined criteria, such as, the specificrequirements of the patient being treated.

A controller 306 can be used to control the specific instructionsregarding the stimulation pulses delivered to the heart 100. In onepossible embodiment, the controller 306 can be controlled manually. Inan alternative embodiment, however, the controller 306 can be controlledautomatically using, for example, feedback received from an intrinsicsignal analyzer 338. Moreover, one having ordinary skill in the art willreadily appreciate that the controller 306 and the programmer 301 can becombined into a single unit. The instructions from the controller 306are received by an electrode switching and output circuitry module 308that delivers the stimulation pulses to the appropriate lead 320 withinthe heart 100.

As discussed above, the heart 100 is connected to the CRT system 300using various leads 320. The various leads 320 are preferably configuredto carry the CRT stimuli from the CRT device to the heart 100. Moreover,the various leads 320 can likewise operate in a demand mode, thereby,relaying intrinsic cardiac signals from the heart's 100 electricalconduction system back to one or more sense amplifiers 310, 312, 314,316. In one possible embodiment, the various leads 320 comprise separateand distinct leads connecting the CRT system 300 to different portionsof the heart 100. In particular, the various leads 320 can comprise alead 322 connected to the right-side portion or pump 102 (FIG. 1) of theheart 100, including, for example, a right atrium lead 324 configured tooperate with a right atrium amplifier 310 and a right ventricle lead 326configured to operate with a right ventricle amplifier 312. Similarly,the various leads 320 can comprise a lead 327 connected to the left-sideportion or pump 104 (FIG. 1) of the heart 100, including, for example, afirst left ventricle lead 328 configured to operate with a first leftventricle amplifier 314 and a second left ventricle lead 330 configuredto operate with a second left ventricle amplifier 316.

As discussed above, the various leads 320 connected to the heart 100 canrelay intrinsic cardiac signals from the heart's 100 electricalconduction system back to the one or more sense amplifiers 310, 312,314, 316. The intrinsic cardiac signals amplified by the senseamplifiers 310, 312, 314, 316 can then be processed by an intrinsicsignal analyzer 338 incorporated in whole or in part by an implantableheart stimulation device (i.e., CRT device) or a device programmer. Theintrinsic signal analyzer 338 generally can comprise a detection module340 that is configured to analyze the intracardiac electrograminformation to detect the beginning and ending of ventriculardepolarization, such as the Q* and S* values discussed above withreference to FIG. 3.

Calculating Q* and S* from the intracardiac electrogram signal may bedone in various ways. See for example, the calculation of Q* from U.S.Pat. No. 6,144,880, which is commonly assigned to Cardiac Pacemakers,Inc. and is incorporated herein by reference. In one embodiment,calculating Q* and S* may proceed as follows. For Q*, a waveform V(n)including the QRS complex must be acquired and analyzed, such as by thedetection module 340 of the CRT device or CRT device programmer. Theacquisition involves digitizing the waveform V(n) including the activitybeginning at the time of an atrial reference marker indicating the endof atrial activity and extending beyond the QRS complex received by theelectrode in the left or right ventricle and storing it in memory of theCRT device or CRT device programmer. Then, Q* is found by the followingprocess.

First, the detection module 340 smooths the waveform V(n). This may bedone by smoothing the waveform V(n) seven times using a 5 pointrectangular moving window (for a sampling frequency of 500 Hz) wherebythe 5 samples for each window are averaged and the average is assignedto the middle sample of the five. A derivative dV(n)/dt of the smoothedwaveform is taken, and the absolute value of the derivative dV(n)/dt isnormalized to range from 0 to 1.

The time samples n from the atrial reference marker time T_(p) to thetime T_(R) of the peak of the R wave of the QRS complex are analyzed.This analysis involves calculating the mean and standard deviation ofboth the smoothed waveform V(n) and the normalized absolute value of itsderivative dV(n)/dt for each time sample within a 50 ms moving window.The baseline window with the minimum mean (i.e., baseline mean) plus abaseline standard deviation for |dV(n)/dt| is found and its values areused in the following steps.

For each sample n between T_(p) and T_(R), if the baseline mean is lessthan |dV(n)/dt|, but more than or equal to |dV(n)/dt|, then the numberof data points N in another 50 ms window is found. N is the accumulationof each data point nw where |dV(nw)/dt| is greater than the baselinemean plus the baseline standard deviation. The window sample nw of thisother window ranges from n to n plus the total number of data points inthe window.

If N divided by the total number of data points in the window is greaterthan 0.96 and T_(q)=0 then set T_(q) equal to n0−1, where T_(q) is thecurrent result of sample time for Q* and n0 is the time sample of thefirst data point that contributes to N. If the total number of datapoints in the window minus N is greater than or equal to 2, then T_(q)is reset to zero. After this is completed for all values of n betweenT_(p) and T_(R), then the final value of T_(q) is used as Q*. Thisprocess may be repeated to obtain a value of Q* for several beats, suchas 16, and the median of these Q* values may be used in the computationof the ventricular depolarization interval. It may be desirable toinclude Q* values in the median determination for beats where theinterval from R wave peak to R wave peak between beats has a variationwithin 10%.

For S*, the same process may be repeated but the time samples n rangingfrom the time T_(p+1) which occurs after sensing atrial activity in thenext cycle until the time T_(R) of the peak of the R wave of the QRScomplex of the current cycle are analyzed rather than the samplesoccurring prior to the R wave peak. Once the process discussed above hasbeen completed for all values starting at T_(p+1) and continuing toT_(R) (i.e., working backwards through the samples with respect totime), the final value of T_(q) is used as S*. As with Q*, this processfor S* may be repeated to obtain a value of S* for several beats, suchas 16, and the median of these S* values may be used in the computationof the ventricular depolarization interval.

After analysis of the electrogram information to find the beginning andending of ventricular depolarization such as Q* and S*, a processingmodule 342 may compute the duration of depolarization and compare it toa threshold value, such as 175 milliseconds, in accordance with themethod described below with reference to FIG. 10 to validate the patientas a responder or non-responder. A configuration module 344 can be usedto make adjustments to the CRT system 300 based upon whether theprocessing module 342 determines the patient to be a responder ornon-responder. The adjustments may include setting the atrioventriculardelay of the CRT device to about one-half of the intrinsic value forresponders or to approximately the intrinsic value for non-responders.For embodiments where the device programmer includes all or part of theintrinsic signal analyzer 338, the device programmer may send aninstruction through telemetry 302 to the implanted heart stimulationdevice to set the atrioventricular delay.

The method of the present disclosure can be implemented using a CRTsystem as shown in FIG. 9 comprising various devices and/or programmers,including implantable or external CRT devices and/or programmers such asa CRT tachy or brady system. Accordingly, the method of the presentdisclosure can be implemented as logical operations controlling asuitable CRT device and/or programmer. The logical operations of thepresent disclosure can be implemented: (1) as a sequence of computerimplemented steps running on the CRT device and/or programmer; and (2)as interconnected machine modules within the CRT device and/orprogrammer.

The implementation is a matter of choice dependant on the performancerequirements of the CRT device and/or programmer implementing the methodof the present disclosure and the components selected by or utilized bythe users of the method. Accordingly, the logical operations making upthe embodiments of the method of the present disclosure described hereincan be referred to variously as operations, steps, or modules. It willbe recognized by one of ordinary skill in the art that the operations,steps, and modules may be implemented in software, in firmware, inspecial purpose digital logic, analog circuits, and any combinationthereof without deviating from the spirit and scope of the presentinvention as recited within the claims attached hereto.

FIG. 10 shows an exemplary embodiment 346 of the logical operations ofthe processing module 342. The process begins by the processing module342 receiving the Q* and S* values from the signals measured bydetection module 340 at receive operation 348. At interval operation350, the processing module 342 computes the time interval between the Q*and S* values. At query operation 352, the processing module 342compares the Q*S* interval to the threshold, such as 175 milliseconds.

If the processing module 342 determines that Q*S* is greater than thethreshold, then the processing module 342 selects an atrioventriculardelay that is about one-half of the intrinsic atrioventricular delay atdelay operation 354. If the processing module 342 determines that Q*S*is less than or equal to the threshold, then the processing module 342selects an atrioventricular delay that is approximately equal to theintrinsic atrioventricular delay at delay operation 356. It is desirableat delay operation 356 to set the atrioventricular delay to theintrinsic atrioventricular delay value less a small delay factor ofabout 30 milliseconds. The configuration module 344 then implements theatrioventricular delay selected by processing module 342 when applyingCRT or other pacing therapy to the patient.

While the invention has been particularly shown and described withreference to preferred embodiments thereof, it will be understood bythose skilled in the art that various other changes in the form anddetails may be made therein without departing from the spirit and scopeof the invention.

1. A system comprising: a module that stores information indicative ofwhether a wide QRS interval is present; and a heart stimulation device,coupled to the module that stores information indicative of whether thewide QRS interval, between the beginning of the intrinsic ventriculardepolarization and the ending of the intrinsic ventriculardepolarization, is present, the heart stimulation device configured toset a paced atrio-ventricular delay to be substantially less than anintrinsic atrio-ventricular delay of the patient when the wide QRSinterval is present.